MiRNA-221-5p promotes breast cancer progression by regulating E-cadherin expression

X.-Y. Niu, Z.-Q. Zhang, P.-L. Ma

Department of Thyroid and Breast Surgery, Bayannur City Hospital, Bayannur, China. 117695468@qq.com

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• Oncology

OBJECTIVE: To elucidate the role of miRNA-221-5p in the development of breast cancer (BCa) and its underlying mechanism.

PATIENTS AND METHODS: The expression level of miRNA-221-5p in 52 pairs of BCa tissues and adjacent normal tissues was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The correlation between miRNA-221-5p expression and pathological indicators of BCa was analyzed. MiRNA-221-5p expression in BCa cells was also determined by qRT-PCR. After transfection of miRNA-221-5p inhibitor in MCF-7 and SKBR3 cells, we detected the regulatory effects of miRNA-221-5p on cellular behaviors through cell counting kit-8 (CCK-8), wound healing, and transwell assay. Finally, the relationship between miRNA-221-5p and E-cadherin in BCa was elucidated.

RESULTS: QRT-PCR results showed that the expression level of miRNA-221-5p in BCa tissues was markedly higher than that in normal tissues. Compared with BCa patients with low expression of miRNA-221-5p, those with high expression had a higher incidence of lymph node metastasis and distant metastasis. However, miRNA-221-5p expression did not correlate with age and sex of BCa patients. MiRNA-221-5p was also highly expressed in BCa cells. Transfection of miRNA-221-5p inhibitor suppressed proliferative, invasive, and migratory potentials of BCa cells. Subsequently, we verified that E-cadherin was lowly expressed in BCa cells, and negatively correlated with miRNA-221-5p. In addition, rescue experiments confirmed that transfection of si-E-cadherin reversed the inhibitory role of miRNA-221-5p knockdown in migratory and invasive potentials of BCa cells.

CONCLUSIONS: The expression of miRNA-221-5p remained high in BCa, which was correlated with lymph node metastasis, distant metastasis, and poor prognosis of BCa. MiRNA-221-5p may promote the invasive and migratory potentials of BCa by regulating E-cadherin expression.

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